Our research plans are based on observations that vitamin A deficiency and protein malnutrition retard or prevent development of some mucosal cells which are known to be involved in producing secretory component and immunoglobulin A. The production of secretory lgA (S-lgA) should be retarded at the same time that malnutrition increases susceptibility to mucosal infection. Our main objective is to achieve an understanding of decreased mucosal immunity in marginally- malnourished and malnourished children and thus provide a basis for the therapeutic control of this immune deficiency. We will extensively evaluate mucosal immunity in malnourished children by quantitating immunologically active compounds secreted: primarily S-lgA as well as lysozyme, aminopeptidase, lgG and total protein concentration. We plan to apply this knowledge to mothers and their children where prevalent malnutrition can be monitored for months without treatment to: a) define persistence of the consequences of maternal malnutrition on infant mucosal immunity; b) determine duration of depressed mucosal immunity after a child's renutrition; c) assess the therapeutic value of vitamin A supplementation before mucosal immunization; d) attempt to measure effects of mucosal vaccines on lymphocyte depletion and S-lgA production. With our guinea pig model and Gunea Pig Inclusion Conjunctivitis we will correlate mucosal disease resistance and the secretory immune response. We plan to measure the effects of vitamin A and/or protein- calorie deficiencies in the young guinea pig by: a) determining changes in resistance to a mucosal infection, Guinea Pig Inclusion Conjunctivitis; b) quantitating S-lgA and bactericidal enzymes concentrations in tears; c) modifying a microassay to measure mucosal cellular immunity; d) determining the duration of depressed mucosal immune mechanisms after nutritional therapy.